Hypertension, Atherosclerosis & Dyslipidaemia Flashcards

1
Q

What is atherosclerosis?

A

Occlusion of a blood vessel caused by the formation of an atheroma between the tunica media and tunica intima

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2
Q

What is the composition of an atheroma?

A

Necrotic mass:

  • lipids
  • inflammatory cell debris (foam cells, macrophages)

Fibrous cap covering the necrotic mass composed of cells and a connective tissue matrix:

  • cells: smooth muscle, foam cells, macrophages, lymphocytes
  • connective tissue matrix: collagen, elastin, proteoglycans
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3
Q

What are the steps of an atheroma formation?

A
  1. Damage to tunica intima of arterial wall
  2. LDLs enter hole in tunica intima and begin building up between tunica intima and tunica media
  3. Inflammatory response occurs and becomes chronic, inflammatory cells flock to area
  4. Necrotic mass formed by original lipids and inflammatory cell debris forms
  5. Fibrous cap develops over necrotic mass
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4
Q

What are risk factors for atherosclerosis?

A

Dyslipidaemia (abnormal deposits of LDLs)

Hypertension (turbulent blood flow more likely to damage tunica intima)

Smoking (cellular damage and inflammatory response)

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5
Q

What are the implications of atherosclerosis?

A

Narrowing of arterial walls

  • increased TPR and BP
  • increased turbulence of blood flow and increased risk of further atheroma deposits
  • decreased blood flow / ischaemia if occlusion becomes severe

Development of thrombus if atherosclerotic plaque ruptures

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6
Q

What is dyslipidaemia?

A

Abnormal concentrations of LDL and HDL lipoproteins and/or triglycerides in the bloodstream

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7
Q

What is the difference between LDL and HDL cholesterol?

A

LDL = low density lipoprotein

  • low protein, high lipid
  • deliver cholesterol from lipid stores to peripheral tissues (“bad” cholesterol)

HDL = high density lipoprotein

  • high protein, low lipid
  • transport cholesterol from peripheral tissues to liver for excretion
  • “good” cholesterol, high levels are protective
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8
Q

What are lipoproteins and triglycerides?

A

Lipoproteins:
- protein complexes that transport lipids (cholesterol, triglycerides and phospholipids) in blood stream

Triglycerides:

  • major form of fat storage in the body
  • 3 molecules of fatty acid and 1 molecule of glycerol
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9
Q

What are considered high ratios of LDL, cholesterol and triglyceride in the body?

A

LDL > 3.5
Cholesterol total > 5.5
Triglyceride > 1.7

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10
Q

What are 5 types of medication used to treat dyslipidaemia?

A
  1. Statins
    - lower production of cholesterol and LDL cholesterol particularly
    - inhibit enzyme HMG-CoA reductase (synthesizes production of cholesterol)
    - increase number of LDL receptors on liver cells
  2. Cholesterol reabsorption inhibitors
  3. Bile acid sequestrants
    - prevents reabsorption of bile in GI tract, body has to use LDLs to replace bile
  4. Nicotinic acid derivatives
    - nicotinic acid (niacin / B3) increases HDL levels
  5. Fibric acid derivatives
    - inhibit production of LDL
    - increase production of HDL
    - increases removal of triglycerides from bloodstream
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11
Q

What is hypertension?

A

Consistently high blood pressure

> 140/90 Grade 1 hypertension

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12
Q

What is the difference between primary and secondary hypertension?

A

Primary / idiopathic:

  • no specific aetiology (complex mix of many factors)
  • 90%

Secondary:

  • secondary to another condition (usually renal or endocrine)
  • 10%
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13
Q

What factors can cause primary hypertension?

A

Conditions that increases cardiac output or total peripheral resistance:

  • SNS dominance
  • RAAS dysfunction
  • insulin resistance
  • imbalance between vasoconstrictors and vasodilators
  • atherosclerosis
  • hypertension
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14
Q

What are clinical findings of hypertension?

A

Blood pressure reading

Retinopathy (fundal changes caused by vessel dilation / haemorrhage)

Bruits and murmurs (turbulent blood flow)

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15
Q

What are the 4 drug classes used to manage hypertension?

A
  1. Statins:
    (HMG-CoA reductase inhibitors)
    - lipid lowering medications
  2. ACE Inhibitors:
    (angiotensin-converting inhibitor)
    - decrease activation of RAAS system
  3. Angiotensin II receptor blockers
    - decrease activation of RAAS system
  4. Beta blockers
    - block activation of B1 receptors in heart (SA node and myocardium)
  5. Calcium channel blockers
    - prevents calcium from entering smooth muscle of heart and blood vessels
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